中文摘要：

气道上皮损伤修复过程包括细胞延伸、迁移和增殖。IQGAP1（IQ domain GTPase-activating protein1）是一个在许多细胞生命活动中非常有意义的蛋白，但其在肺上皮细胞中的作用尚未阐述清楚。本文采用目前广泛应用的刮伤气道上皮细胞的体外模型来研究IQGAP1的功能。结果显示，IQGAP1在小鼠、大鼠、猪和人气道上皮细胞中有丰富表达。它与微管骨架共定位，可被微管解聚剂nocodazole破坏。刮伤6-9h后，IQGAP1 mRNA及蛋白表达上调。过表达外源性IQGAP1导致β-catenin核转位，从而活化Tcf／Lef信号。此外，刮伤还影响IQGAP1与β-catenin、结肠腺瘤病（adenomatous polyposis coli，APC）蛋白及细胞质连接蛋白-170（cytoplasmic linker protein-170，CLIP-170）之间的相互作用。通过小于扰RNA（small interference RNA，siRNA）沉默IQGAP1表达则明显延迟损伤愈合。结果提示，IQGAP1信号参与气道上皮细胞损伤修复过程。

英文摘要：

The process of injury and repair in airway epithelium involves cell spreading and migration followed by cell proliferation. IQ domain GTPase-activating protein 1 （IQGAP 1） acts in a series of cell processes, but has not been clarified in lung epithelial cells. In this study, a widely used model of injury and repair in vitro by scratching bronchial epithelial cells （BECs） was utilized to investigate the function of IQGAP 1. The results showed that IQGAP 1 was abundant in BECs of mouse, rat, pig and human. IQGAP 1 was colocalized with tubulin cytoskeleton, but was destroyed by nocodazole, a microtubule disassembly reagent. IQGAP1 mRNA and protein expressions increased at 6-9 h after scratching. In addition, overexpression of IQGAP1 translocated β-catenin from the cytoplasm into the nucleus and activated the Tcf/Lef signal. Scratching altered the associations of IQGAP1 with β-catenin, adenomatous polyposis coli （APC） and cytoplasmic linker protein-170 （CLIP-170）. Silencing IQGAP1 expression by small interference RNA （siRNA） blocked the wound closure. It is concluded that IQGAP 1 signal is involved in the wound closure of BECs induced by scratching.